8/12/2019 Deep Tissue Injury-White-Paper.pdf

1/4

Deep Tissue Injury

Overview

Deep tissue injury is a term proposed by NPAUP to describe a unique form of

pressure ulcers. These ulcers have been described by clinicians for many years with termssuch as purple pressure ulcers, ulcers that are likely to deteriorate and bruises on bony

prominences (Ankrom, 2005). NPAUPs proposed definition, is A pressure-relatedinjury to subcutaneous tissues under intact skin. Initially, these lesions have the

appearance of a deep bruise. These lesions may herald the subsequent development of aStage III-IV pressure ulcer even with optimal treatment.(NPAUP, 2002).

Why is it important to have another label for pressure ulcers? Arent four stages

enough? Perhaps not, because deep tissue injury represents a dangerous lesion due to itspotential for rapid deterioration. Proper labeling will afford clinicians a more accuratediagnosis, and lay a foundation for the development of efficacious interventions.

Background

Shea (1975) is often credited with labeling the stages of pressure ulcers, and his

descriptions of four depths of ulcers were adapted by IAET, AHCPR, and NPUAP.Missing from that four stage system label is deep tissue injury. However, Shea did not

forget them in his review. He described ulcers that appear innocent yet conceal a deep,potentially fatal lesion. In 1873 Paget may have been the first to describe deep tissue

injury describing purple areas with sloughing of tissue and large cavities once they open.In 1942, Groth created deep, malignant pressure sores in an animal model in a series of

experiments that began in deeper tissues and spread to the surface.The reasons for the rapid deterioration seen with deep tissue injury may be a

combination of direct ischemic injury and reperfusion injury from oxygen free radicals,cytokines and neutrophilic adhesion to microvascular endothelium. When there is a long

duration of ischemia, the "direct" damage resulting from hypoxia alone is thepredominant mechanism. With shorter periods of ischemia, the indirect or reperfusion

mediated damage becomes increasingly more important. For example, it has been shownin an animal model that the intestinal injury induced by 3 hours of ischemia (flow

reduced to 20% of normal) and one hour of reperfusion is several times greater than that

observed after 4 hours of ischemia alone (Parks & Granger, 1988). These resultsdemonstrate that the injury produced by reperfusion can be more severe than the injuryinduced by ischemia per se. This same pattern of relative contribution of injury from

direct and indirect mechanisms has been shown to occur in the heart, brain, muscle andother organs. Since the body of reperfusion injury literature suggests that significant

damage occurs upon reperfusion, the development of methods to block the chemical andbiological mediators of reperfusion injury holds promise for treating many conditions

even perhaps pressure ulcers.

8/12/2019 Deep Tissue Injury-White-Paper.pdf

2/4

8/12/2019 Deep Tissue Injury-White-Paper.pdf

3/4

Bruise: the extravasation of blood in the tissues as a result of blunt force impactto the body. Usually about two weeks is required for healing a bruise under normal

conditions. History of trauma is common.

Calciphylaxis: vascular calcification and skin necrosis most common in patients

with a long-standing history of chronic renal failure and renal replacement therapy.

Lesions may have a violaceous hue and be excruciatingly tender and extremely firm.Lesions are most commonly seen on the lower extremities, not bony prominences. Theincidence of these lesions is very low in general patient populations.

Hematoma: deep seated purple nodule from clotted blood, usually associated withtrauma.

Fourniers gangrene: intensely painful necrotizing fasciitis of the perineum. May

present initially as cellulites .

Perirectal Abscess: commonly presents as a dull, aching, or throbbing pain in the

perianal area. The pain worsens when sitting and immediately before defecation; the painabates after defecation. A tender fluctuant mass may be palpated at the anal verge. These

abscesses can open to reveal large cavities which can be confused with deep pressureulcers.

Implications for research

It is imperative that research be conducted on pressure-related deep tissue injury.While these lesions were likely included in much previous work on pressure ulcer

prevalence, incidence, and natural history, since staging system definitions have beenambiguous in how to characterize deep tissue injury under intact skin, the epidemiology

and clinical course of these lesions remains unknown. Prospective observational studies

can lead to a full understanding of the likelihood of deterioration versus completeresolution, and will allow an unambiguous nomenclature to be developed with respect toreliably diagnosing and predicting the natural history of these lesions.

A second area for research are studies designed to develop diagnostic methods toidentify the extent of tissue damage under intact skin (e.g., depth, volume) as well as the

viability of injured tissue (e.g., viable, necrotic). These methods may be particularlyapplicable to patients with darkly-pigmented skin in whom the visual signs of deep tissue

injury can be hard to identify.A third area for research is to identify the most efficacious treatments for each

type of deep tissue injury. Interventions should be tested that can prevent further damage,salvage injured yet viable tissue, and maximize overall healing rates.

Implications for education

Education is imperative to assist all health care providers to conduct thorough

skin assessments, and understand how to use a precise nomenclature to describe thephenomenon of deep tissue injury.

8/12/2019 Deep Tissue Injury-White-Paper.pdf

4/4

Regulatory issues

A full understanding of the nature of deep tissue injury and the efficaciousmethods for treatment should guide the regulation of payment, as well as the

implementation of sanctions for suboptimal care.

Questions:

What are the clinical indicators that you would use to define a stage I pressure ulcer?

How can deep tissue injury be best identified in patients with darkly-pigmented skin?How long does it take to develop a deep tissue injury?

What level of pressure/stress is required to develop a deep tissue injury?How do co-morbidities (esp. rapid weight loss, loss of sensation) affect the time to

develop deep tissue injury?Does a deep tissue injury that never reaches the skin really a pressure ulcer?

How would a revised staging system affect documentation?

How would a revised staging system impact regulation and reimbursement?How would the addition of deep tissue injury to the nomenclature of pressure ulcers

affect liability?

How would a revised staging system impact health care quality measures?

References

Ankrom, M., Bennett, R., Sprigle, S., Langemo, D., Black, J., Berlowicz, D., Lyder, C.,and the National Pressure Ulcer Advisory Panel (2005). Pressure-related deep tissue

injury under intact skin and the current pressure ulcer staging systems. Advances in Skinand Wound Care 18, (in press).

Black, J. (2003). Deep tissue injury. Wounds: A compendium of clinical research andpractice 15 (11), 380.

Groth, K.E. (1942). Clinical observations and experimental studies of the pathogenesis ofdecubitus ulcers. Acta Chir Scand 76 (supple), 1-209.

Husain, T. (1953). An experimental study of some pressure effects on tissues, withreference to the bedsore problem. Journal of Pathology and Bacteria 66, 347-358.

Shea, J.D. (1975) Pressure sores. Clinical Orthopedics and Related Research 112, 89-100.Willms-Kretschmer, K. & Majno, G. (1969). Ischemia of the skin. American Journal of

Pathology 54 (5), 327-341.Giordano C.P., Scott D., Koval, K.J., et al. (1995). Fracture blister formation: a

laboratory study. Journal of Trauma 38 (6) 907-9McCann S. & Gruen G. (1997). Fracture blisters: a review of the literature. Orthopaedic

Nursing 16(2) 17-22Paget J. (1873). Clinical lecture on bed-sores. Student Journal and Hospital Gazette May

10, 144-146.Parks, D.S.& Granger, D.N. (1988). Ischemia-reperfusion injury: a radical view.

Hepatology 8 (3), 680-682.Russell, L. (2002). Pressure ulcer classification: Defining early skin damage. British

Journal of Nursing 11 (916), S33-S41.